Chronic Heart failure is defined as the inability of the heart to maintain adequate cardiac output and blood pressure to meet the bodies requirements. It can be caused in a number of ways including Ischaemic Heart Disease, Hypertension, Valvular disease, Cardiomyopathy & a number of less common causes. It is a common condition and causes huge amounts of disability and mortality. Treatment costs for heart failure & it’s consequences is estimated to account for 2% of the NHS budget.

Symptoms & Signs

Depend upon which ventricle is affectedSymptoms from LVF & RVF often overlap, so don’t worry if you have a mixed pictureThe most common cause of RVF is LVF therefore patients often present with bothIf both the left & right ventricle are affected, this is known as Congestive heart failureSymptomsLeft ventricular failureDyspnoeaFatigueOrthopnoeaParoxysmal nocturnal dyspnoeaNocturnal cough - pink frothy sputumWheezeCold peripheriesPoor exercise tolerance

Diagnosis is achieved through interpretation of a number of investigationsEchocardiography is the most useful in giving a specific diagnosis.The heart failure is then classified using the New York Classification of Heart Failure;

The term “heart failure” makes it sound like the heart is no longer working at all and there’s nothing that can be done. Actually, heart failure means that the heart isn’t pumping as well as it should be. Congestive heart failure is a type of heart failure that requires seeking timely medical attention, although sometimes the two terms are used interchangeably. With heart failure, the weakened heart can’t supply the cells with enough blood. This results in fatigue and shortness of breath and some people have coughing. Everyday activities such as walking, climbing stairs or carrying groceries can become very difficult. Heart failure is a term used to describe a heart that cannot keep up with its workload. The body may not get the oxygen it needs.Heart failure is a serious condition, and usually there’s no cure. But many people with heart failure lead a full, enjoyable life when the condition is managed with heart failure medications and healthy lifestyle changes. It’s also helpful to have the support of family and friends who understand your condition.

How the normal heart works

The normal healthy heart is a strong, muscular pump a little larger than a fist. It pumps blood continuously through the circulatory system.

Watch an animation of blood flow through the heart.

The heart has four chambers, two on the right and two on the left:

Two upper chambers called atria (one is called an atrium) Two lower chambers called ventricles

The right atrium takes in oxygen-depleted blood from the rest of the body and sends it back out to the lungs through the right ventricle where the blood becomes oxygenated.

Oxygen-rich blood travels from the lungs to the left atrium, then on to the left ventricle, which pumps it to the rest of the body.

The heart pumps blood to the lungs and to all the body’s tissues through a sequence of highly organized contractions of the four chambers. For the heart to function properly, the four chambers must beat in an organized way. At first the heart tries to make up for this by:

Enlarging. The heart stretches to contract more strongly and keep up with the demand to pump more blood. Over time this causes the heart to become enlarged. Developing more muscle mass. The increase in muscle mass occurs because the contracting cells of the heart get bigger. This lets the heart pump more strongly, at least initially. Pumping faster. This helps increase the heart’s output.

The body also tries to compensate in other ways:

The blood vessels narrow to keep blood pressure up, trying to make up for the heart’s loss of power. The body diverts blood away from less important tissues and organs (like the kidneys), the heart and brain.

These temporary measures mask the problem of heart failure, but they don’t solve it. Heart failure continues and worsens until these compensating processes no longer work.

Eventually the heart and body just can’t keep up, and the person experiences the fatigue, breathing problems or other symptoms that usually prompt a trip to the doctor.

The body’s compensation mechanisms help explain why some people may not become aware of their condition until years after their heart begins its decline. (It's also a good reason to have a regular checkup with your doctor.)

Heart failure can involve the heart’s left side, right side or both sides. However, it usually affects the left side first.

Heart failure is a pathophysiological state in which cardiac output is insufficient to meet the needs of the body and lungs. The term "congestive heart failure" is often used, as one of the common symptoms is congestion, or build-up of fluid in a person's tissues and veins in the lungs or other parts of the body.

********Heart failure is a multisystem disorder which is characterised by abnormalities of cardiac, skeletal muscle, and renal function; stimulation of the sympathetic nervous system; and a complex pattern of neurohormonal changes. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1128747/

Myocardial systolic dysfunction#The primary abnormality in non-valvar heart failure is an impairment in left ventricular function, leading to a fall in cardiac output. The fall in cardiac output leads to activation of several neurohormonal compensatory mechanisms aimed at improving the mechanical environment of the heart .Activation of the # sympathetic system, for example, tries to maintain cardiac output with : an @ increase in heart rate,@ increased myocardial contractility,@ increased peripheral vasoconstriction (increased catecholamines). Activation of# the renin-angiotensin-aldosterone system (RAAS) also results in @ vasoconstriction *(angiotensin) and an @ increase in blood volume, with retention of # salt and water *(aldosterone). Concentrations of # vasopressin and # natriuretic peptides increase. Furthermore, there may be @ progressive cardiac dilatation or @ alterations in cardiac structure (remodelling), or both.

Neurohormonal activation#Chronic heart failure is associated with neurohormonal activation and alterations in autonomic control. Although these compensatory neurohormonal mechanisms provide valuable support for the heart in normal physiological circumstances, they also have a fundamental role in the development and subsequent progression of chronic heart failure.Renin-angiotensin-aldosterone systemStimulation of the renin-angiotensin-aldosterone system leads to increased concentrations of : renin, plasma angiotensin II, and aldosterone. Angiotensin II is : a potent vasoconstrictor of the * renal (efferent arterioles) and * systemic circulation, where it stimulates release of noradrenaline from sympathetic nerve terminals,@ inhibits vagal tone, and promotes the release of aldosterone. This leads to the * retention of sodium and water and the increased * excretion of potassium. In addition, angiotensin II has important effects on cardiac myocytes and may contribute to the * endothelial dysfunction that is observed in chronic heart failure.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1128747/

The sympathetic nervous system is activated in heart failure, via low and high pressure baroreceptors, as an early compensatory mechanism which provides * inotropic support and maintains * cardiac output. Chronic sympathetic activation, however, has deleterious effects, causing a further * deterioration in cardiac function.

The earliest increase in sympathetic activity is detected in the heart, and this seems to precede the increase in sympathetic outflow to skeletal muscle and the kidneys that is present in advanced heart failure. Sustained sympathetic stimulation activates the @ renin-angiotensin-aldosterone system and other neurohormones, leading to * increased venous (PRE) and arterial (AFTER) tone (and greater preload and afterload respectively),* increased plasma noradrenaline concentrations, progressive * retention of salt and water, and oedema. Excessive sympathetic activity is also associated with cardiac myocyte apoptosis, hypertrophy, and focal myocardial necrosis.In the long term, the ability of the myocardium to respond to chronic high concentrations of catecholamines is attenuated by a down regulation in β receptors, although this may be associated with baroreceptor dysfunction and a further increase in sympathetic activity. Indeed, @ abnormalities of baroreceptor function are well documented in chronic heart failure, along with reduced @ parasympathetic tone, leading to abnormal autonomic modulation of the sinus node. Moreover, a reduction in heart rate variability has consistently been observed in chronic heart failure, as a result of predominantly sympathetic and reduced vagal modulation of the sinus node, which may be a prognostic marker in patients with chronic heart failure.

Natriuretic peptidesThere are three natriuretic peptides, of similar structure, and these exert a wide range of effects on the heart, kidneys, and central nervous system.Atrial natriuretic peptide (ANP) is * released from the atria * in response to stretch, leading to * natriuresis and * vasodilatation. In humans, brain natriuretic peptide (BNP) is also released from the heart, predominantly from the ventricles, and its actions are similar to those of atrial natriuretic peptide.C-type natriuretic peptide is limited to the vascular endothelium and central nervous system and has only limited effects on natriuresis and vasodilatation.

The atrial and brain natriuretic peptides * increase in response to volume expansion and pressure overload of the heart and act * as physiological antagonists to the effects of angiotensin II on vascular tone, aldosterone secretion, and renal-tubule sodium reabsorption. As the natriuretic peptides are important mediators, with increased circulating concentrations in patients with heart failure, interest has developed in both the diagnostic and prognostic potential of these peptides. Substantial interest has been expressed about the therapeutic potential of natriuretic peptides, particularly with the development of agents that inhibit the enzyme that metabolises atrial natriuretic peptide (neutral endopeptidase), and non-peptide agonists for the A and B receptors.

Skeletal muscle changesConsiderable peripheral changes occur in the skeletal muscle of patients with chronic heart failure. These include a @ reduction in muscle mass and @ abnormalities in muscle *structure, *metabolism, and *function. There is also reduced @ blood flow to active skeletal muscle, which is related to vasoconstriction and the loss in muscle mass. All these abnormalities in skeletal muscles, including respiratory muscles, contribute to the symptoms of fatigue, lethargy, and exercise intolerance that occur in chronic heart failure.

Diastolic dysfunctionDiastolic dysfunction results from @ impaired myocardial relaxation, with increased * stiffness in the ventricular wall and * reduced left ventricular compliance, leading to * impairment of diastolic ventricular filling. Infiltrations, such as amyloid heart disease, are the best examples, although coronary artery disease, hypertension (with left ventricular hypertrophy), and hypertrophic cardiomyopathy are more common causes Neurohormonal mechanisms and compensatory mechanisms in heart failure